In the last four decades, a rapid increase could be observed in the Western industrial countries in metabolic disturbances, especially in disturbances of the fat metabolism. The main reason for this is excessive nutrition and/or too fatty foods with simultaneous lack of movement. Under these conditions, increased cholesterol and lipid values may form in the blood, which increase the risk arteriosclerotic, cardiac and peripheral vascular diseases. It is known that increased blood cholesterol levels are co-responsible for the emergence of arterial vascular sclerosis. Hypercholesteraemia is a metabolic disturbance which always accompanies hyperlipidaemia. The pathogenetically different but symptomatically similar clinical pictures of hyperlipidaemia (turbidity of the serum by chylomicrons) and of hypercholesteraemia (increase of the cholesterol content in the blood plasma to more than 200 mg %) are summarized under the collective concepts hyperlipoproteinaemia or hyperlipidaemia.
For the treatment of hypercholesteraemia, predominantly aryloxyacetic acid derivates, especially alpha-(p-chlorophenoxy)-isobutyric acid-ethylesters, as well as nicotinic acid derivatives are used.
In addition, DE-PS 24 61 742 of the applicant describes the use of pyridoxin-5'-phosphoric acid ester-glutaminates and -asparaginates for the treatment and prophylaxis of hypercholesteraemia.
Without it being necessary for the clinical picture of hypercholesteraemia or hyperlipidaemia to be present, in the case of an endangered group of persons, namely smokers, diabetics, ageing persons and those with high blood pressure or persons who are exposed to great stress, vascular lesions may occur. This is traced back to the presence of an increased concentration of peroxides in the blood, which are bonded by LDL (low density lipoprotein). These LDL-bonded peroxides cause and accelerate the formation of atheromae and arteriosclerotic plaques in the vessels and can be regarded as the cause of diabetic angiopathy. The presence of increased concentrations of peroxidizing products and their correlation with vascular lesions is described by J. M. C. Gutteridge et al. in Trends in Biochemical Sciences, April 1990, pages 129 to 135 and by D. W. Morel et al. in Journal of Lipid Research, Vol. 30, 1989, pages 1827 to 1834.
It is known that the arteriosclerotic changes in the vessels are a result of endothelial lesions, and the pathogenesis proceeds as follows: endolethelial lesion-platelet adhesion-proliferation of smooth muscle cells-lipid deposit.
The first step, the endolethial lesion, may have a plurality of causes, namely mechanical damage due to shearing forces in the case of hypertonia, chemical damage due to cholesterol in hypercholesteraemia and in particular toxic damage due to contaminants in the blood. It is assumed that the further course is almost identical with all three types of damage.
The consequence of an endothelial lesion as well as of the subsequent fat deposit between and in the cells of the arterial intima is an increased aggregation of thrombocytes, accompanied by a proliferation of smooth muscle cells, caused by the further increased inflow of lipoproteins in the connective tissue basic substance, where complex formation with glucose aminoglycans of the connective tissue and metabolic defects result on the cellular level. Then the formation of calcium in the damaged zones forms the conclusion of all the changes, which, in the final analysis, lead to a constriction of the vessels.
Tests were carried out on hypercholesteremic rabbits and rats by W. Schneider in his dissertation concluded in 1987 at the Johannes Gutenberg University of Mainz, which showed that when administering relatively high concentrations of magnesium-pyridoxal-5'-phosphate-glutaminate (MPPG), the liver and aorta lipid concentrations are reduced. But this work does not provide any indications with reference to the mechanism which initiates the vessel atheroma formation in the endangered groups of persons, so that on the basis of the results of W. Schneider, it cannot be concluded that an atheroma formation can be prevented by the elimination of the initiating contaminants in the blood.
For some time past it has been suspected that peroxides in the blood may function as the initiators of metabolic disturbances. U. P. Steinbrecher et al. describe in J. Biol. Chem., Vol. 264, No. 26, pages 15216 to 15223 (1989) the presence of oxidizingly modified LDL as well as a receptor for it. The applicant has now proven in purposeful tests that this concerns LDL-bonded peroxides. By tests made in vitro one of the mechanisms underlying toxic endothelial lesion could be clarified and it was shown that it is possible to intercept these peroxides and to render them harmless.